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Top 10 Cardio Drugs 2012 – FiercePharma

May 21, 2013 by 2012pharmaceutical

See on Scoop.it – Cardiotoxicity

Top 10 Cardio Drugs 2012
FiercePharma
According to EvaluatePharma’s World Preview 2018 report, combined sales of antihypertensive drugs and antihyperlipidemics were more than $70 billion in 2011. That would put them at the top of the heap.

See on www.fiercepharma.com

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Scientists unite to solve mystery of mental illness and neurological conditions – Wellcome Trust

May 21, 2013 by 2012pharmaceutical

See on Scoop.it – Cardiovascular Disease: PHARMACO-THERAPY

Wellcome Trust Scientists unite to solve mystery of mental illness and neurological conditions Wellcome Trust Professor Adrian Harwood, who leads research into the emerging field of cellular pharmacology, which examines the interaction of…

See on www.wellcome.ac.uk

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Resistant Hypertension Responds to Renal Denervation – Renal and Urology News

May 21, 2013 by 2012pharmaceutical

See on Scoop.it – Cardiovascular Disease: PHARMACO-THERAPY

Resistant Hypertension Responds to Renal Denervation
Renal and Urology News
During the studies, all of the patients remained on their antihypertensive regimen; however, changes in their regimens were allowed as clinically indicated.

See on www.renalandurologynews.com

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Novel Approach to Resistant Hypertension Reported – Renal and Urology News

May 21, 2013 by 2012pharmaceutical

See on Scoop.it – Cardiotoxicity

Novel Approach to Resistant Hypertension Reported
Renal and Urology News
In a prospective, single-arm, open-label trial, Dr.

See on www.renalandurologynews.com

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JNC 2013: Simplified BP Goal in Sight – MedPage Today – MedPage Today

May 21, 2013 by 2012pharmaceutical

See on Scoop.it – Cardiotoxicity

JNC 2013: Simplified BP Goal in Sight – MedPage Today MedPage Today “Based on recent guidelines, but not necessarily JNC-8, the degree of blood pressure reduction achieved, and not the initial antihypertensive class of agents chosen, is more…

See on www.medpagetoday.com

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The Most Expensive Hospital in America – Becker’s Hospital Review

May 21, 2013 by 2012pharmaceutical

See on Scoop.it – Cardiovascular and vascular imaging

ThinkProgress The Most Expensive Hospital in America Becker’s Hospital Review Bayonne typically charged $99,689 for treating each case of chronic lung disease, which is five times as much as other hospitals and 17 times as much as Medicare paid in…

See on www.beckershospitalreview.com

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Salivary Gland Cancer – Adenoid Cystic Carcinoma: Mutation Patterns: Exome- and Genome-Sequencing @ Memorial Sloan-Kettering Cancer Center

May 20, 2013 by 2012pharmaceutical

Reporter: Aviva Lev-Ari, PhD, RN

 

Researchers Report on Mutational Patterns in Adenoid Cystic Carcinoma

May 20, 2013

NEW YORK (GenomeWeb News) – A Memorial Sloan-Kettering Cancer Center-led team has taken an exome- and genome-sequencing centered look at the mutations that may be found in the salivary gland cancer adenoid cystic carcinoma, or ACC.

As they reported in Nature Genetics online yesterday, the researchers did exome or genome sequencing on five-dozen matched ACC tumor and normal pairs.

Their analysis unearthed relatively few glitches in each tumor’s protein-coding sequences. But the group found suspicious mutations to several main pathways, including some — such as the PI3-kinase, fibroblast growth factor, and insulin-like growth factor-containing pathway — that may make promising treatment targets.

“Our discovery of genomic alterations in targetable pathways suggests potential avenues for novel treatments to address a typically chemoresistant malignancy,” corresponding author Timothy Chan, an oncology researcher at Memorial Sloan-Kettering, and his colleagues wrote, noting that “[v]erified ACC cell lines are needed to further substantiate the clinical usefulness of the mutations identified here.”

A few genetic glitches have been linked to ACC in the past, the team noted, including a fusion between the transcription factor genes MYB and NFIB. The tumors are also notorious for having higher-than-usual expression of certain genes, such as the epidermal growth factors. Even so, there is still a ways to go in characterizing and treating the aggressive cancer.

To get a better sense of the nature and frequency of mutations involved in ACC, the researchers used Illumina’s HiSeq2000 to do exome sequencing on 55 matched ACC and normal samples, as well as whole-genome sequencing on five more tumor-normal pairs.

For the exome sequencing experiments, they used Agilent SureSelect kits to capture protein-coding portions of the genome prior to sequencing. In the subsequent analyses, meanwhile, the group relied on Life Tehnologies’ SOLiD and Illumina’s MiSeq platforms to verify apparent single nucleotide glitches and small insertions and deletions.

With 106-fold coverage of the exomes, on average, and 37-fold average coverage of the genomes, the group was able to track down a mean of almost two-dozen somatic coding alterations per tumor.

When they used an algorithm called CHASM to distinguish between driver and passenger mutations in a set of 710 validated non-synonymous mutations, the researchers saw an over-representation of apparent driver mutations affecting genes known for processes ranging from chromatin regulation and DNA damage response to signaling and metabolism.

For instance, more than one-third of the tumors harbored mutations to chromatin regulators or chromatin state modifying genes such as SMARCA2, CREBBP, and KDM6A. Similarly, the researchers tracked down multiple mutations to genes coding for enzymes involved in adding or removing methylation and acetylation marks to histones.

Glitches to DNA damage response pathways also turned up in multiple tumors, they reported, as did mutations involving genes from the FGF-IGF-PI3K and other signaling pathways.

Some 57 percent of the tumors tested contained the MYB-NFIB fusion that had been implicated in ACC previously. But the new analysis also turned up mutations affecting genes that interact with MYB and in the NFIB gene itself, pointing to widespread — and perhaps complex — involvement for the two transcription factors in ACC.

“Our data highlight MYB as an active oncogenic partner in fusion transcripts in ACC,” the study’s authors said, “but also suggest a separate role for NFIB, given the presence of mutations specific to this gene.”

Going forward, the group hopes to see further analyses on alterations uncovered in the current study, particularly those falling in pathways that might be prone to clinical interventions.

“[O]ur data provide insights into the genetic framework underlying ACC oncogenesis,” the researchers concluded, “and establish a foundation for identifying new therapeutic strategies.”

 

 

Posted in Biological Networks, Gene Regulation and Evolution, CANCER BIOLOGY & Innovations in Cancer Therapy, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Chemical Genetics, Computational Biology/Systems and Bioinformatics, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Genome Biology, Genomic Testing: Methodology for Diagnosis, Metabolomics, Molecular Genetics & Pharmaceutical, Personalized and Precision Medicine & Genomic Research, Regulated Clinical Trials: Design, Methods, Components and IRB related issues | Tagged , , , , | 1 Comment »

Long-Term Mortality in Treated Hypertensive Patients: Serum Uric Acid Level, Longitudinal Blood Pressure and Renal Function

May 20, 2013 by 2012pharmaceutical

Reporter: Aviva Lev-Ari, PhD, RN

 

 

  • Original Article

HYPERTENSIONAHA.113.00859 Published online before print May 20, 2013,doi: 10.1161/​HYPERTENSIONAHA.113.00859

Serum Uric Acid Level, Longitudinal Blood Pressure, Renal Function, and Long-Term Mortality in Treated Hypertensive Patients
  1. Jesse Dawson,
  2. Panniyammakal Jeemon,
  3. Lucy Hetherington,
  4. Caitlin Judd,
  5. Claire Hastie,
  6. Christin Schulz,
  7. William Sloan,
  8. Scott Muir,
  9. Alan Jardine,
  10. Gordon McInnes,
  11. David Morrison,
  12. Anna Dominiczak,
  13. Sandosh Padmanabhan,
  14. Matthew Walters

+Author Affiliations


  1. From the Institute of Cardiovascular and Medical Sciences (J.D., P.J., L.H., C.J., C.H., C.S., S.M., A.J., G.M., A.D., S.P., M.W.), West of Scotland Cancer Surveillance Unit (W.S., D.M.), College of Medical, Veterinary & Life Sciences, University of Glasgow, Glasgow, United Kingdom.
  1. Correspondence to Matthew Walters, Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary & Life Sciences, Western Infirmary, University of Glasgow, Glasgow G11 6NT, United Kingdom. E-mail matthew.walters@glasgow.ac.uk; or Sandosh Padmanabhan, BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, 126 University Pl, University of Glasgow, Glasgow G12 8TA, United Kingdom. E-mail Sandosh.padmanabhan@glasgow.ac.uk

Abstract

Uric acid may have a role in the development of hypertension and renal dysfunction. We explored the relationship among longitudinal blood pressure, renal function, and cardiovascular outcomes in a large cohort of patients with treated hypertension. We used data from the Glasgow Blood Pressure Clinic database. Patients with a baseline measure of serum uric acid and longitudinal measures of blood pressure and renal function were included. Mortality data were obtained from the General Register Office for Scotland. Generalized estimating equations were used to explore the relationship among quartiles of serum uric acid, blood pressure, and estimated glomerular filtration rate. Cox proportional hazard models were developed to assess mortality relationships. In total, 6984 patients were included. Serum uric acid level did not influence the longitudinal changes in systolic or diastolic blood pressure but was related to change in glomerular filtration rate. In comparison with patients in the first quartile of serum uric acid, the relative decrease in glomerular filtration rate in the fourth was 10.7 (95% confidence interval, 7.9–13.6 mL/min per 1.73 m2) in men and 12.2 (95% confidence interval, 9.2–15.2 mL/min per 1.73 m2) in women. All-cause and cardiovascular mortality differed across quartiles of serum uric acid in women only (P<0.001; hazard ratios for all-cause mortality 1.38 [95% confidence interval, 1.14–1.67] for the fourth quartile of serum uric acid compared with the first). Serum uric acid level was not associated with longitudinal blood pressure control in adults with treated hypertension but was related to decline in renal function and mortality in women.

Key Words:

  • Received February 19, 2013.
  • Revision received April 23, 2013.
  • Accepted April 23, 2013.

http://hyper.ahajournals.org/content/early/2013/05/20/HYPERTENSIONAHA.113.00859.abstract.html?papetoc

 

Posted in Bio Instrumentation in Experimental Life Sciences Research, Biomarkers & Medical Diagnostics, Bone Disease and Musculoskeletal Disease, Chemical Biology and its relations to Metabolic Disease, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Frontiers in Cardiology and Cardiovascular Disorders, HTN, Human Sensation and Cellular Transduction: Physiology and Therapeutics | Tagged , , , | 1 Comment »

Prediction of Occurrence of Cardiovascular Events Independently of Left Ventricular Mass in Hypertensive Patients: Monitoring of Timing of Korotkoff Sounds as Indicator of Arterial Stiffness

May 20, 2013 by 2012pharmaceutical

Reporter: Aviva Lev-Ari, PhD, RN
  • Original Article

HYPERTENSIONAHA.113.01039 Published online before print May 20, 2013,doi: 10.1161/​HYPERTENSIONAHA.113.01039

Arterial Stiffness From Monitoring of Timing of Korotkoff Sounds Predicts the Occurrence of Cardiovascular Events Independently of Left Ventricular Mass in Hypertensive Patients

  1. Philippe Gosse,
  2. Antoine Cremer,
  3. Georgios Papaioannou,
  4. Sunthareth Yeim

+Author Affiliations


  1. From the Department of Cardiology and Hypertension, University Hospital of Bordeaux, Bordeaux, France.
  1. Correspondence to Philippe Gosse, Department of Cardiology and Hypertension, University Hospital of Bordeaux, Hopital Saint Andre, 1 Rue Jean Burguet, 33075 Bordeaux, France. E-mail philippe.gosse@chu-bordeaux.fr

Abstract

Several studies have established that the increase in arterial stiffness (AS) is a cardiovascular risk factor but to date no studies have evaluated in hypertensive patients its prognostic value in comparison with another powerful risk factor, left ventricular mass (LVM) as measured by echocardiography. We prospectively evaluated the prognostic value of AS and LVM in patients with essential hypertension. The population studied comprised 793 patients (56% men) aged 54±14 years. For 519 patients, baseline measurements were made before any antihypertensive treatment, for 274 patients, the measurement were obtained during the follow-up period under antihypertensive treatment. AS was assessed from ambulatory monitoring of blood pressure and timing of Korottkoff sounds. Left ventricular mass was measured in 523 patients. After a mean follow-up of 97 months, 122 cardiovascular events were recorded in the whole population and 74 in the group with LVM determination. AS as continuous or discontinuous variable was independently related to cardiovascular events. The existence or not of antihypertensive treatment at the time of its measurement did not affect its prognostic value. When LVM was forced in the model, AS remained significantly related to cardiovascular events. Thus, AS has an independent prognostic value in the hypertensive, whether measured before or after the administration of antihypertensive treatment. This prognostic value persists after taking LVM into account.

Key Words:

  • Received January 10, 2013.
  • Revision received March 25, 2013.
  • Accepted April 22, 2013.

http://hyper.ahajournals.org/content/early/2013/05/20/HYPERTENSIONAHA.113.01039.abstract.html?papetoc

Posted in Atherogenic Processes & Pathology, Frontiers in Cardiology and Cardiovascular Disorders, HTN, Origins of Cardiovascular Disease | Tagged , , , , , | 1 Comment »

Echo vs Cardiac Magnetic Resonance Imaging (CMRI): CMRI may be a useful adjunct in Hypertrophic Cardiomyopathy (HCM) family screening in higher risk

May 20, 2013 by 2012pharmaceutical

Reporter: Aviva Lev-Ari, PhD, RN

 

  • Original Article

Comparison of Echocardiographic and Cardiac Magnetic Resonance Imaging in Hypertrophic Cardiomyopathy Sarcomere Mutation Carriers without Left Ventricular Hypertrophy

  1. Anne Marie Valente1,
  2. Neal K. Lakdawala2,
  3. Andrew J. Powell3,
  4. Sarah P. Evans3,
  5. Allison L. Cirino4,
  6. E. J. Orav4,
  7. Calum A. MacRae4,
  8. Steven D. Colan3 and
  9. Carolyn Y. Ho4*

+Author Affiliations


  1. 1Brigham and Women’s Hospital & Boston Children’s Hospital, Boston, MA

  2. 2Brigham and Women’s Hospital & VA Boston Healthcare System, Boston, MA

  3. 3Boston Children’s Hospital, Boston, MA

  4. 4Brigham and Women’s Hospital, Boston, MA
  1. ↵* Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115 cho@partners.org

Abstract

Background—Left ventricular hypertrophy (LVH) typically manifests during or after adolescence in sarcomere mutation carriers at risk for developing hypertrophic cardiomyopathy (HCM). Guidelines recommend serial imaging of mutation carriers without LVH (G+/LVH-) to monitor for phenotypic evolution, but the optimal strategy is undefined. Compared with echocardiography (echo), cardiac magnetic resonance imaging (CMR) offers improved endocardial visualization and potential to assess scar. However the incremental advantage offered by CMR for early diagnosis of HCM is unclear. Therefore, we systematically compared echo and CMR in G+/LVH- subjects.

Methods and Results—Forty sarcomere mutation carriers with normal echo wall thickness (< 12 mm or z-score < 2.5 in children) underwent concurrent CMR. Mean age was 21.7 ± 11.1 years, 55% were female). If LV wall thickness appeared non-uniform, the size and location of relatively thickened segments were noted. Late gadolinium enhancement (LGE) was assessed with CMR. Diagnostic agreement between echo and CMR was good (90%), although CMR measurements of LV wall thickness were ~19% lower than echo. Four subjects had mild hypertrophy (12.6-14 mm, ≤2 segments) appreciated by CMR but not echo. No subjects had LGE. During median 35-month follow up, 2 subjects developed overt HCM, including 1 with mild LVH by CMR at baseline.

Conclusions—Echo is unlikely to miss substantial LVH; however CMR identified mild hypertrophy in ~10% of mutation carriers with normal echo wall thickness. CMR may be a useful adjunct in HCM family screening, particularly in higher risk situations, or if echocardiographic images are suboptimal or suggest borderline LVH.

Key Words:

Received July 10, 2012.

Revision received April 25, 2013.
Accepted May 3, 2013.

 

Posted in Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Medical Imaging Technology, Image Processing/Computing, MRI, CT, Nuclear Medicine, Ultra Sound | Tagged , , , | Leave a Comment »

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